ABP1 Modulation of Ubiquitin mediated protein degradation in Cell Cycle and Auxin Signalling – AMUCCAS

Plant growth and developmental processes are controlled by the action of plant hormones amongst which auxin is implicated in virtually every aspects. In some tissues, auxin promotes cell division while in others the hormone regulates cell elongation or cell differentiation. In the 80s, the Auxin Binding Protein 1 (ABP1) was identified on its capacity to bind auxin. Many characteristics of ABP1 are consistent with receptor function however little is known on its mode of action. Recent identification of another auxin receptor, TIR1, an F-box protein involved in the SCF complex mediating the degradation of transcriptional repressors (IAA/Aux), has raised number of questions concerning the relative role of each receptors in auxin signalling. Partner 1 has recently highlighted that ABP1 is interfering with the degradation of IAA/Aux proteins, suggesting a functional relationship between ABP1 and SCFTIR1. In addition, P1 has recently demonstrated that ABP1 is essential for auxin control of cell division. Our working hypothesis is that ABP1 acts via the modulation of distinct ubiquitin mediated protein degradation pathways. Primary data supports that a key cell cycle target of ABP1 could be E2F transcription factors. The project aims at elucidating the mode of action of ABP1 on both auxin and cell cycle related protein degradation pathways. We will focus on one hand on the relationship of ABP1 with SCFTIR1 and its substrates IAA/Aux and on the other hand on E2Fs turnover and the identification of the ubiquitin E3 ligase responsible for their degradation. For the first time, molecular and genetic tools required to place ABP1 in the complex network of auxin signalling are available. Bearing in mind the critical importance of auxin in plants, it is essential to understand the fine tuning of its mechanisms of action. Results expected within this project will undoubtedly improve this understanding and will shed new lighting on our knowledge of auxin signalling and its control on the cell cycle.